in both L. salmonis (up to 140-fold) [122] and C. rogercresseyi (up to 13-fold)
[118]. Several studies have endeavored to quantify resistance levels among L.
salmonis as well as to identify genetic adaptive changes that are mechanistically
responsible for decreased pyrethroid sensitivity. In general, experiments to discern
resistance phenotypes from sensitive ones involve a time-to-impairment measurement (ET 50 ) with a discriminating dose of pyrethroid or the derivation of a concentration (EC 50 ) that elicits the desired effect (e.g., immobility, detachment from fish)
based on a dose-response [123]. In at least some populations, resistance has been
maintained stably for at least 3–4 years after bringing populations into a pyrethroidfree laboratory setting, suggesting an adaptive response. The median effective
concentration (EC 50 ) of deltamethrin needed to treat resistant and susceptible strains
of L. salmonis from Scotland sometimes differed by over 140-fold [124]. The high
magnitude of differential sensitivity between strains suggests an adaptive mechanism (see Ffrench-Constant et al. [101]). To date, no single mechanism has been
identified to explain the stark differences in sensitivity among resistant and sensitive
strains of L. salmonis although several studies have identified nuclear [115, 125] and
mitochondrial [124, 126] markers that have been correlated with resistance, and a
resistant phenotype seems to result from a combination of both nuclear and mitochondrial changes. Fallang et al. [125] identified a novel point mutation in the
domain II (S5) region of the para-type Vgsc (LsN v 1.1) that produced a glutamineto-arginine amino acid substitution at position 945 (Q945R, Musca domestica
numbering) that was prominent in L. salmonis populations with documented control
failures and absent from sensitive populations. However, that amino acid substitution was not documented in other resistant populations [115] nor had it been
previously documented in resistant pest insects, leaving its functional role in target
site insensitivity tenuous. Carmona-Antonanzas et al. [115] searched for potential
kdr-type mutations in three different L. salmonis sodium channel homologues. The
authors identified several non-synonymous base pair substitutions in one (LsN v 1.3)
of the sodium channel homologues among two resistant sea lice populations,
sometimes at high frequencies (0.80). One mutation, an isoleucine-to-valine substitution at position 936 (I936V; M. domestica numbering), was absent in two sensitive
populations of L. salmonis, supporting its role in conferring resistance (Fig. 4)
[115]. While evidence for the I936V playing a role in pyrethroid resistance is
limited, this mutation has been previously associated with pyrethroid resistance in
the corn earworm [127] and has shown a capacity to decrease pyrethroid binding
when mutant channels from Drosophila melanogaster were cloned into Xenopus
oocytes and subjected to voltage clamp analysis [128]. Interestingly, isoleucine at
this position is usually present in arthropods, while valine is typically present in
vertebrates, potentially providing evidence for lineage-specific differences in
sensitivity [129].
Two studies have demonstrated that pyrethroid resistance in L. salmonis has a
strong maternal component, potentially mediated through some form of
mitochondrial-based inheritance. Carmona-Antonanzas et al. [124] crossed the
resistant (140-fold) and sensitive strains of L. salmonis from Scotland and reared
offspring out to the third filial (F1 to F3) generation. When F2 organisms came from
The Ecological and Evolutionary Implications of Pyrethroid Exposure: A New. . .
121
[118]. Several studies have endeavored to quantify resistance levels among L.
salmonis as well as to identify genetic adaptive changes that are mechanistically
responsible for decreased pyrethroid sensitivity. In general, experiments to discern
resistance phenotypes from sensitive ones involve a time-to-impairment measurement (ET 50 ) with a discriminating dose of pyrethroid or the derivation of a concentration (EC 50 ) that elicits the desired effect (e.g., immobility, detachment from fish)
based on a dose-response [123]. In at least some populations, resistance has been
maintained stably for at least 3–4 years after bringing populations into a pyrethroidfree laboratory setting, suggesting an adaptive response. The median effective
concentration (EC 50 ) of deltamethrin needed to treat resistant and susceptible strains
of L. salmonis from Scotland sometimes differed by over 140-fold [124]. The high
magnitude of differential sensitivity between strains suggests an adaptive mechanism (see Ffrench-Constant et al. [101]). To date, no single mechanism has been
identified to explain the stark differences in sensitivity among resistant and sensitive
strains of L. salmonis although several studies have identified nuclear [115, 125] and
mitochondrial [124, 126] markers that have been correlated with resistance, and a
resistant phenotype seems to result from a combination of both nuclear and mitochondrial changes. Fallang et al. [125] identified a novel point mutation in the
domain II (S5) region of the para-type Vgsc (LsN v 1.1) that produced a glutamineto-arginine amino acid substitution at position 945 (Q945R, Musca domestica
numbering) that was prominent in L. salmonis populations with documented control
failures and absent from sensitive populations. However, that amino acid substitution was not documented in other resistant populations [115] nor had it been
previously documented in resistant pest insects, leaving its functional role in target
site insensitivity tenuous. Carmona-Antonanzas et al. [115] searched for potential
kdr-type mutations in three different L. salmonis sodium channel homologues. The
authors identified several non-synonymous base pair substitutions in one (LsN v 1.3)
of the sodium channel homologues among two resistant sea lice populations,
sometimes at high frequencies (0.80). One mutation, an isoleucine-to-valine substitution at position 936 (I936V; M. domestica numbering), was absent in two sensitive
populations of L. salmonis, supporting its role in conferring resistance (Fig. 4)
[115]. While evidence for the I936V playing a role in pyrethroid resistance is
limited, this mutation has been previously associated with pyrethroid resistance in
the corn earworm [127] and has shown a capacity to decrease pyrethroid binding
when mutant channels from Drosophila melanogaster were cloned into Xenopus
oocytes and subjected to voltage clamp analysis [128]. Interestingly, isoleucine at
this position is usually present in arthropods, while valine is typically present in
vertebrates, potentially providing evidence for lineage-specific differences in
sensitivity [129].
Two studies have demonstrated that pyrethroid resistance in L. salmonis has a
strong maternal component, potentially mediated through some form of
mitochondrial-based inheritance. Carmona-Antonanzas et al. [124] crossed the
resistant (140-fold) and sensitive strains of L. salmonis from Scotland and reared
offspring out to the third filial (F1 to F3) generation. When F2 organisms came from
The Ecological and Evolutionary Implications of Pyrethroid Exposure: A New. . .
121